miRNA-22 suppresses colon cancer cell migration and invasion by inhibiting the expression of T-cell lymphoma invasion and metastasis 1 and matrix metalloproteinases 2 and 9

Li, Bo; Song, Yan; Liu, Tongjun; Cui, Youbin; Jiang, Yang; Xie, Zhixun; Xie, Songqiang

doi:10.3892/or.2013.2300

Cited by 52 publications

(49 citation statements)

References 38 publications

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“…2D) [26]. Further, we estimated the expression level of NET1 by qRT-PCR in PBMCs of CML patients (patient subset [14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30]. The results showed that the level of NET1 was significantly higher in all the patients compared with that of the control cells validating the results obtained using cell lines (Fig.…”

Section: Mir-22 Is Downregulated In Chronic Myeloid Leukemia Cellssupporting

confidence: 65%

“…It is downregulated in gastric cancer and thought to be involved in invasion and migration [13]. A high miR-22 level is also known to suppress colon, ovarian and lung cancer progression and hypoxia signaling in colon cancer cells [14][15][16][17]. All these studies strongly indicate that miR-22 is a tumor suppressor, but its precise role and the mechanisms involved have not been addressed so far.…”

Section: Introductionmentioning

confidence: 99%

“…A list of predicted targets is shown in Table 1. These putative targets were further substantiated by determining the expression of target genes and [14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30]. Graphical data points denote mean AE SD (t test, ***P ≤ 0.001).…”

Section: Mir-22 Is Downregulated In Chronic Myeloid Leukemia Cellsmentioning

confidence: 99%

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miR‐22 regulates expression of oncogenic neuro‐epithelial transforming gene 1, NET1

et al. 2014

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MicroRNAs control cellular processes by regulating expression of their target genes. Here we report that neuro-epithelial transforming gene 1 (NET1) is a target of tumor suppressor microRNA 22 (miR-22). miR-22 is downregulated in peripheral blood mononuclear cells derived from chronic myeloid leukemia (CML) patients and in CML cell line K562. NET1 was identified as one of the targets of miR-22 using both in vitro and in vivo experiments. Either mutations or naturally occurring single-nucleotide polymorphisms in NET1 3 0 -UTR that map at the miR-22 binding site were found to affect binding of miR-22 to NET1 mRNA. Over expression of NET1 in K562 cells resulted in increased proliferation. However decreased proliferation and alteration in cell cycle were observed on either overexpression of miR-22 or knockdown of NET1 expression respectively. We also found that overexpression of miR-22 or NET1 knockdown inhibits actin fiber formation, probably by downregulation of NET1 as NET1 knockdown also resulted in depletion of actin fiber formation. We suggest that the oncogenic properties of CML cells are probably due to deregulated expression of NET1 as a result of altered expression of miR-22.

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Section: Mir-22 Is Downregulated In Chronic Myeloid Leukemia Cellssupporting

confidence: 65%

Section: Introductionmentioning

confidence: 99%

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miR‐22 regulates expression of oncogenic neuro‐epithelial transforming gene 1, NET1

et al. 2014

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“…It has been shown that miR-22 induces senescence of neonatal rat cardiac fibroblasts by modulating the expression of mimecan (osteoglycin, OGN) [23]. In cancer cell lines, miR-22 inhibits cell proliferation by targeting MYCBP (c-Myc-binding protein) [24], p21(CDKN1A) [25], ErbB3 [26], TIAM1 (T-cell lymphoma invasion and metastasis 1) [27] and Sp1 [28] and restores cellular senescence by targeting the senescence-associated genes CDK6, SIRT1 and Sp1 [29]. Conversely, miR-22 promotes tumorigenesis and metastasis by directly targeting the PI3K/AKT inhibitor PTEN (phosphatase tensin and homolog) [30,31] and the TET (Ten eleven translocation) family of methylcytosine dioxygenases [32,33].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-22 Induces Endothelial Progenitor Cell Senescence by Targeting AKT3

Zheng

2014

Cell Physiol Biochem

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Objectives: Endothelial progenitor cells (EPCs) play an important role in postnatal neovascularization. The number and function of EPCs declines as part of aging-associated senescence, thereby potentially contributing to vascular pathologies. Here, we investigated the significance and molecular mechanisms of microRNA-22 (miR-22) governing EPC senescence. Methods: EPCs were isolated from human circulating mononuclear cells from healthy young and aged volunteers. Cell senescence, proliferation, migration and tube formation ability were detected by SA-β-gal staining assay, MTT assay, transwell assay and Matrigel-based angiogenesis assay. Gene and protein expression were analyzed by qRT-PCR and Western blot respectively. Results: We found that miR-22 was upregulated in aged EPCs. Overexpression of miR-22 in young EPCs induced cell senescence, decreased proliferation and migration, and impaired angiogenesis in vitro. Conversely, silencing of endogenous miR-22 led to decreased cell senescence, increased proliferation and migration, and improved angiogenesis. AKT3 was identified as a direct target of miR-22, and restoration of AKT3 expression attenuated the effects of miR-22 in young EPCs. Conclusion: Our results indicate that miR-22 induces EPC senescence by downregulating AKT3 expression, providing a potential novel target for the reversal of EPC dysfunction in angiogenesis.

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“…The activated form of STAT5 drives miR-155 expression, which in turn promotes proliferation of malignant T cells [27] indicating that miR-155 plays an oncomiR function in CTCL. In contrast, miR-22 is recognized as a tumor suppressor and is down-regulated in CTCL [35, 36] as well as in several other cancer types [37, 38]. …”

Section: Introductionmentioning

confidence: 99%

STAT5 induces miR-21 expression in cutaneous T cell lymphoma

et al. 2016

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In cutaneous T cell lymphomas (CTCL), miR-21 is aberrantly expressed in skin and peripheral blood and displays anti-apoptotic properties in malignant T cells. It is, however, unclear exactly which cells express miR-21 and what mechanisms regulate miR-21. Here, we demonstrate miR-21 expression in situ in both malignant and reactive lymphocytes as well as stromal cells. qRT-PCR analysis of 47 patients with mycosis fungoides (MF) and Sezary Syndrome (SS) confirmed an increased miR-21 expression that correlated with progressive disease. In cultured malignant T cells miR-21 expression was inhibited by Tofacitinib (CP-690550), a clinical-grade JAK3 inhibitor. Chromatin immunoprecipitation (ChIP) analysis showed direct binding of STAT5 to the miR-21 promoter. Cytokine starvation ex vivo triggered a decrease in miR-21 expression, whereas IL-2 induced an increased miR-21 expression in primary SS T cells and cultured cytokine-dependent SS cells (SeAx). siRNA-mediated depletion of STAT5 inhibited constitutive- and IL-2-induced miR-21 expression in cytokine-independent and dependent T cell lines, respectively. IL-15 and IL-2 were more potent than IL-21 in inducing miR-21 expression in the cytokine-dependent T cells. In conclusion, we provide first evidence that miR-21 is expressed in situ in CTCL skin lesions, induced by IL-2 and IL-15 cytokines, and is regulated by STAT5 in malignant T cells. Thus, our data provide novel evidence for a pathological role of IL-2Rg cytokines in promoting expression of the oncogenic miR-21 in CTCL.

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miRNA-22 suppresses colon cancer cell migration and invasion by inhibiting the expression of T-cell lymphoma invasion and metastasis 1 and matrix metalloproteinases 2 and 9

Cited by 52 publications

References 38 publications

miR‐22 regulates expression of oncogenic neuro‐epithelial transforming gene 1, NET1

miR‐22 regulates expression of oncogenic neuro‐epithelial transforming gene 1, NET1

MicroRNA-22 Induces Endothelial Progenitor Cell Senescence by Targeting AKT3

STAT5 induces miR-21 expression in cutaneous T cell lymphoma

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